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Epstein-Barr virus growth-transformed cells are converted to malignancy following transfection of a 1.3-kb CATR1 antisense construct independent of a change in the level of c-myc expression followed by a 8;14 chromosomal translocation.爱泼斯坦-巴尔病毒生长转化细胞在转染1.3 kb的CATR1反义构建体后会转变为恶性肿瘤，这一过程与c-myc表达水平的变化无关，随后会发生8；14染色体易位。
Proc Natl Acad Sci U S A. 1998 Apr 28;95(9):4894-9. doi: 10.1073/pnas.95.9.4894.
2
Malignant conversion of human cells by antisense cDNA to a putative tumor suppressor gene.通过反义互补DNA将人类细胞恶性转化为一个假定的肿瘤抑制基因。
Carcinogenesis. 1996 Aug;17(8):1751-5. doi: 10.1093/carcin/17.8.1751.
3
Cloning and sequencing of CATR1.3, a human gene associated with tumorigenic conversion.与致瘤性转化相关的人类基因CATR1.3的克隆与测序
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4
c-myc activation renders proliferation of Epstein-Barr virus (EBV)-transformed cells independent of EBV nuclear antigen 2 and latent membrane protein 1.c-myc激活使爱泼斯坦-巴尔病毒（EBV）转化的细胞增殖独立于EBV核抗原2和潜伏膜蛋白1。
Proc Natl Acad Sci U S A. 1996 Sep 17;93(19):10411-6. doi: 10.1073/pnas.93.19.10411.
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A human T lymphotropic virus type I (HTLV-I) long terminal repeat-directed antisense c-myc construct with an Epstein-Barr virus replicon vector inhibits cell growth in a HTLV-I-transformed human T cell line.一种带有爱泼斯坦-巴尔病毒复制子载体的人I型嗜T淋巴细胞病毒（HTLV-I）长末端重复序列定向反义c-myc构建体可抑制HTLV-I转化的人T细胞系中的细胞生长。
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Growth and spread in nude mice of Epstein-Barr virus transformed B-cells from a chronic lymphocytic leukemia patient.一名慢性淋巴细胞白血病患者的爱泼斯坦-巴尔病毒转化B细胞在裸鼠体内的生长与扩散
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The Epstein-Barr virus BRLF1 gene product transactivates the murine and human c-myc promoters.爱泼斯坦-巴尔病毒BRLF1基因产物可反式激活小鼠和人类的c-myc启动子。
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c-myc expression is activated by the immunoglobulin kappa-enhancers from a distance of at least 30 kb but not by elements located within 50 kb of the unaltered c-myc locus in vivo.在体内，c-myc表达可被免疫球蛋白κ增强子从至少30kb的距离激活，但不能被位于未改变的c-myc基因座50kb范围内的元件激活。
Oncogene. 1996 Mar 21;12(6):1299-307.
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Malignant conversion of chemically transformed normal human cells.化学转化的正常人细胞的恶性转化
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Changes in levels of normal ML-1 gene transcripts associated with the conversion of human nontumorigenic to tumorigenic phenotypes.与人类非致瘤性向致瘤性表型转变相关的正常ML-1基因转录本水平的变化。
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本文引用的文献

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Myc/Ig juxtaposition by chromosomal translocations: some new insights, puzzles and paradoxes.染色体易位导致的Myc/Ig并置：一些新见解、谜题与悖论
Immunol Today. 1985 Jul;6(7):208-15. doi: 10.1016/0167-5699(85)90036-2.
2
Ineffectiveness of the presence of H-ras/p53 combination of mutations in squamous cell carcinoma cells to induce a conversion of a nontumorigenic to a tumorigenic phenotype.鳞状细胞癌细胞中H-ras/p53联合突变的存在无法诱导非致瘤表型向致瘤表型的转变。
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3
Malignant conversion of human cells by antisense cDNA to a putative tumor suppressor gene.通过反义互补DNA将人类细胞恶性转化为一个假定的肿瘤抑制基因。
Carcinogenesis. 1996 Aug;17(8):1751-5. doi: 10.1093/carcin/17.8.1751.
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Chromosome 7q allelic losses in pancreatic carcinoma.
Cancer Res. 1996 Aug 15;56(16):3808-13.
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Malignant conversion of chemically transformed normal human cells.化学转化的正常人细胞的恶性转化
Proc Natl Acad Sci U S A. 1996 May 28;93(11):5229-34. doi: 10.1073/pnas.93.11.5229.
6
Spontaneous development of a chromosomal translocation 5;14 in an Epstein-Barr-virus-associated B-cell lymphoma in a SCID mouse.严重联合免疫缺陷（SCID）小鼠的爱泼斯坦-巴尔病毒相关B细胞淋巴瘤中5号与14号染色体易位的自发发生
Int J Cancer. 1993 Sep 9;55(2):281-7. doi: 10.1002/ijc.2910550219.
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(C-A)n microsatellite repeat D7S522 is the most commonly deleted region in human primary breast cancer.（C-A）n微卫星重复序列D7S522是人类原发性乳腺癌中最常缺失的区域。
Proc Natl Acad Sci U S A. 1994 Dec 6;91(25):12155-8. doi: 10.1073/pnas.91.25.12155.
8
Loss of heterozygosity in human primary prostate carcinomas: a possible tumor suppressor gene at 7q31.1.人类原发性前列腺癌中的杂合性缺失：7q31.1处可能存在的肿瘤抑制基因。
Cancer Res. 1994 Dec 15;54(24):6370-3.
9
Frequent loss of heterozygosity of the long arm of chromosome 7 is closely associated with progression of human gastric carcinomas.7号染色体长臂杂合性的频繁缺失与人类胃癌的进展密切相关。
Int J Cancer. 1994 Dec 1;59(5):597-600. doi: 10.1002/ijc.2910590504.
10
Frequent loss of heterozygosity in human primary squamous cell and colon carcinomas at 7q31.1: evidence for a broad range tumor suppressor gene.人类原发性鳞状细胞癌和结肠癌中7q31.1位点杂合性频繁缺失：广泛存在的肿瘤抑制基因的证据
Cancer Res. 1995 Mar 15;55(6):1347-50.

爱泼斯坦-巴尔病毒生长转化细胞在转染1.3 kb的CATR1反义构建体后会转变为恶性肿瘤，这一过程与c-myc表达水平的变化无关，随后会发生8；14染色体易位。

Epstein-Barr virus growth-transformed cells are converted to malignancy following transfection of a 1.3-kb CATR1 antisense construct independent of a change in the level of c-myc expression followed by a 8;14 chromosomal translocation.

作者信息

Li D, Sun X L, Casto B, Fang J, Theil K, Glaser R, Milo G

机构信息

Department of Medical Biochemistry, Ohio State University Medical Center, Columbus OH 43210, USA.

出版信息

Proc Natl Acad Sci U S A. 1998 Apr 28;95(9):4894-9. doi: 10.1073/pnas.95.9.4894.

DOI:10.1073/pnas.95.9.4894
PMID:9560199
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC20184/
Abstract

The AGLCL Epstein-Barr virus (EBV) growth-transformed cell line is incapable of inducing tumors in nude mice. When the cells were transfected with a 1.3-kb CATR1 antisense cDNA construct, progressively growing lymphomas could be induced in nude mice. Chromosome analysis of the parental, transfected, and tumor cells revealed that a chromosomal translocation t(8;14)(q24.1;q32) had occurred in the transfected cells and was retained in cells derived from tumors. Moreover, enhanced c-myc expression, usually associated with this translocation, was either unchanged or under-expressed. These data suggest that the malignant transformation of the EBV growth-transformed cells was independent of c-myc expression and suggest that the CATR1 gene may act synergistically with the chromosomal translocation facilitating the conversion of AGLCL cells from a growth-transformed state to a malignant phenotype.

摘要

AGLCL 爱泼斯坦-巴尔病毒（EBV）生长转化细胞系无法在裸鼠中诱导肿瘤形成。当用一个1.3 kb的CATR1反义cDNA构建体转染这些细胞时，可在裸鼠中诱导出逐渐生长的淋巴瘤。对亲本细胞、转染细胞和肿瘤细胞进行染色体分析发现，转染细胞中发生了染色体易位t(8;14)(q24.1;q32)，且该易位在肿瘤来源的细胞中得以保留。此外，通常与这种易位相关的c-myc表达增强要么未改变，要么表达不足。这些数据表明，EBV生长转化细胞的恶性转化独立于c-myc表达，并表明CATR1基因可能与染色体易位协同作用，促进AGLCL细胞从生长转化状态转变为恶性表型。